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  • Product Name: Scutellarin
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27740-01-8

27740-01-8 structure
27740-01-8 structure
  • Name: Scutellarin
  • Chemical Name: scutellarin
  • CAS Number: 27740-01-8
  • Molecular Formula: C21H18O12
  • Molecular Weight: 462.360
  • Catalog: Biochemical Chinese herbal medicine ingredients
  • Create Date: 2018-09-02 01:13:27
  • Modify Date: 2024-01-02 15:41:54
  • Scutellarin, an active flavone isolated from Scutellaria baicalensis, can down-regulates the STAT3/Girdin/Akt signaling in HCC cells, and inhibits RANKL-mediated MAPK and NF-κB signaling pathway in osteoclasts.

Name scutellarin
Synonyms 5,6-Dihydroxy-2-(4-hydroxyphenyl)-4-oxo-4H-1-benzopyran-7-yl-β-D-glucopyranosiduronic acid
Breviscapin Scutellarein-7-O-β-D-glucuronide
Scutellarein-7β-D-glucuronoside
Scutellarein-7β-D-glucuronide
MFCD01861503
Scutellarein 7-O-β-D-glucuronide
Breviscapin
Scutellarin
7-(β-D-Glucopyranuronosyloxy)-5,6-dihydroxy-2-(4-hydroxyphenyl)-4H-1-benzopyran-4-one
Breviscapine
Scutellarein 7-b-D-glucuronide
5,6-Dihydroxy-2-(4-hydroxyphenyl)-4-oxo-4H-chromen-7-yl β-D-glucopyranosiduronic acid
Scutellarein 7-
4H-1-Benzopyran-4-one, 7-(β-D-glucopyranuronosyloxy)-5,6-dihydroxy-2-(4-hydroxyphenyl)-
Scutellarein-7-O-β-D-glucuronide
Description Scutellarin, an active flavone isolated from Scutellaria baicalensis, can down-regulates the STAT3/Girdin/Akt signaling in HCC cells, and inhibits RANKL-mediated MAPK and NF-κB signaling pathway in osteoclasts.
Related Catalog
Target

STAT3

Akt

In Vitro Scutellarin treatment significantly reduces HepG2 cell viability in a dose-dependent manner, and inhibits migration and invasion of HCC cells in vitro. Scutellarin treatment significantly reduces STAT3 and Girders of actin filaments (Girdin) expression, STAT3 and Akt phosphorylation in HCC cells. Introduction of STAT3 overexpression restores the scutellarin-downregulated Girdin expression, Akt activation, migration and invasion of HCC cells. Furthermore, induction of Girdin overexpression completely abrogates the inhibition of scutellarin on the Akt phosphorylation, migration and invasion of HCC cells. Scutellarin can inhibit HCC cell metastasis in vivo, and migration and invasion in vitro by down-regulating the STAT3/Girdin/Akt signaling[1]. Scutellarin selectively enhances Akt phosphorylation[2]. Scutellarin is a putative therapeutic agent as it has been found to not only suppress microglial activation thus ameliorating neuroinflammation, but also enhance astrocytic reaction. Acutellarin amplifies the astrocytic reaction by upregulating the expression of neurotrophic factors among others thus indicating its neuroprotective role. Remarkably, the effects of scutellarin on reactive astrocytes are mediated by activated microglia supporting a functional "cross-talk" between the two glial types[3]. Scutellarin can suppress RANKL-mediated osteoclastogenesis, the function of osteoclast bone resorption, and the expression levels of osteoclast-specific genes (tartrate-resistant acid phosphatase (TRAP), cathepsin K, c-Fos, NFATc1). Further investigation indicates that Scutellarin can inhibit RANKL-mediated MAPK and NF-κB signaling pathway, including JNK1/2, p38, ERK1/2, and IκBα phosphorylation[5].
In Vivo Scutellarin (50 mg/kg/day) significantly mitigates the lung and intrahepatic metastasis of HCC tumors in vivo. The numbers of the lung and intrahepatic metastatic tumors in the scutellarin-treated group are significantly less than that in the controls[1]. The rats treated with Scutellarin display a significant alleviation in neurobehavioral deficits compared to the SAH group. Scutellarin enhanced eNOS expression compared with SAH rats[4].
Cell Assay HepG2 cells (1×105/well) are cultured in 96-well plates and treated in triplicate with scutellarin at concentrations of 5, 10, 20, 30, and 100 μM or vehicle alone for 24 h. The cellular viability is tested by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, and is expressed as a percentage of proliferation versus controls.
Animal Admin To establish an orthotopic liver xenograft model, individual mice are anesthetized with isoflurane and a small incision is made in their abdomen. Individual mice are injected with 2×106 SK-Hep1 cells in 30 μL Matrigel into their left lobe of the liver. Twenty-four hours after orthotopic liver implantation, the mice are randomized and injected intraperitoneally with scutellarin (50 mg/kg/day) or vehicle (0.9% NaCl, normal saline) daily for 35 consecutive days (n=10 per group). Subsequently, the mice are sacrificed, and their lungs and livers are excised, fixed in 10% buffered formalin and paraffin-embedded for hematoxylin and eosin staining.
References

[1]. Ke Y, et al. Scutellarin suppresses migration and invasion of human hepatocellular carcinoma by inhibiting the STAT3/Girdin/Akt activity. Biochem Biophys Res Commun. 2016 Dec 18. pii: S0006-291X(16)32174-X

[2]. Yang LL, et al. Differential regulation of baicalin and scutellarin on AMPK and Akt in promoting adipose cell glucose disposal. Biochim Biophys Acta. 2016 Nov 27;1863(2):598-606.

[3]. Wu CY, et al. Scutellarin attenuates microglia-mediated neuroinflammation and promotes astrogliosis in cerebral ischemia - a therapeutic consideration. Curr Med Chem. 2016 Nov 18. [Epub ahead of print]

[4]. Li Q, et al. Scutellarin attenuates vasospasm through the Erk5-KLF2-eNOS pathway after subarachnoid hemorrhage in rats. J Clin Neurosci. 2016 Dec;34:264-270

[5]. Zhao S, et al. Scutellarin inhibits RANKL-mediated osteoclastogenesis and titanium particle-induced osteolysis via suppression of NF-κB and MAPK signaling pathway. Int Immunopharmacol. 2016 Nov;40:458-465

Density 1.8±0.1 g/cm3
Boiling Point 891.6±65.0 °C at 760 mmHg
Molecular Formula C21H18O12
Molecular Weight 462.360
Flash Point 314.9±27.8 °C
Exact Mass 462.079834
PSA 207.35000
LogP -0.46
Vapour Pressure 0.0±0.3 mmHg at 25°C
Index of Refraction 1.764
Storage condition 2-8°C
RIDADR NONH for all modes of transport

~%

27740-01-8 structure

27740-01-8

Literature: Ono, Eiichiro; Ruike, Miho; Iwashita, Takashi; Nomoto, Kyosuke; Fukui, Yuko Phytochemistry, 2010 , vol. 71, # 7 p. 726 - 735
Precursor  2

DownStream  2